Cardiovascular disease is the leading cause of morbidity and mortality in the United States, causing forty-one percent of all deaths. Following coronary artery occlusion, myocardial recovery is dependent on the heart's ability to develop collateral circulation and revascularize the infarcted myocardium. Although much is known about positive growth factors such as vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) that promote myocardial revascularization following myocardial infarction, the molecular mechanisms opposing these stimuli are unknown (see, e.g., J. Li et al., VEGF, flk-1, and flt-1 expression in a rat myocardial infarction model of angiogenesis, Am J Physiol. 270: H1803-11 (1996); K. Shinohara et al., Expression of vascular endothelial growth factor in human myocardial infarction, Heart Vessels 11 113-22 (1996); M. Miyataka et al., Basic fibroblast growth factor increased regional myocardial blood flow and limited infarct size of acutely infarcted myocardium in dogs, Angiology 49, 381-90 (1998); M. Horrigan et al., Reduction in myocardial infarct size by basic fibroblast growth factor following coronary occlusion in a canine model, Int J Cardiol. 10, S85-91 (1999); D. Losordo et al., Gene therapy for myocardial angiogenesis: initial clinical results with direct myocardial injection of phVEGF165 as sole therapy for myocardial ischemia, Circulation 98, 2800-4 (1998); and U.S. Pat. No. B1 5,661,144 to Leiden et al., (Reexamination Certificate Issued Jun. 1, 1999)). Accordingly, there is a need for new ways to treat cardiovascular disease.